NES and acute myeloid leukemia: Drastic remodelling of endosteal vasculature in AML. Endosteal AML cells produce pro‐inflammatory and anti‐angiogenic factors. Loss of osteoblasts, HSCs and HSC niches. Sympathetic neuropathy blocks the differentiation of Nestin+ MSCs into NG2+ cells. Increased vascular permeability allowing HSC egress from the BM. Overall loss of BM stroma in AML mouse models. Reduced numbers and activity of osteoblasts in AML patients.